Abstract
In airway epithelial cultures, mechanical stimulation induces intracellular Ca2+ concentration ([Ca2+](i)) changes by causing Ca2+ entry and intracellular Ca2+ release. Mechanically induced Ca2+ fluxes across the plasma membrane are blocked by Ni2+ (Boitano, S., M. J. Sanderson, and E. R. Dirksen. J. Cell. Sci. 107: 3037-3044, 1994). In this report we use fluorescence imaging microscopy with fura 2 and intracellular recording of the transmembrane potential to further characterize Ca2+ flux in the plasma membrane of these cells. Mechanically induced Ca2+ influx is blocked by nifedipine. Addition of the dihydropyridine agonist BAY K 8644 (2 μM) leads to a delayed increase of [Ca2+](i) that is dependent on extracellular Ca2+. Switching to high extracellular K+ concentration ([K+](o)) causes depolarization of the plasma membrane and a transient increase in [Ca2+](i). The number of cells that respond to high [K+](o) is significantly decreased by Ni2+ (1 mM) or nifedipine (10 μM). Mechanical stimulation causes a rapid depolarization of the stimulated cell that can be suppressed by the K+ ionophore valinomycin. Valinomycin treatment also blocks mechanically induced Ca2+ flux. These results suggest that voltage- sensitive Ca2+conducting channels exist in airway epithelial cells, and these channels contribute to the [Ca2+](i) changes observed after mechanical stimulation or depolarization of the plasma membrane.
Original language | English (US) |
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Pages (from-to) | C1547-C1556 |
Journal | American Journal of Physiology - Cell Physiology |
Volume | 269 |
Issue number | 6 38-6 |
DOIs | |
State | Published - 1995 |
Externally published | Yes |
Keywords
- dihydropyridine
- mechanical stimulation
- membrane potential
- valinomycin
ASJC Scopus subject areas
- Physiology
- Cell Biology